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40 Cards in this Set

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  • Back
In what form do cyanobacterial heterocysts feed Nitrogen to vegetative cells?
What exchange occurs between heterocysts and vegetative cells in filamentous cyanobacteria?
Vegetative cell gives: glutamate, e- donor for Photosystem I ATP synthesis

Heterocyst gives: glutamine
What two enzyme systems do heterocysts use to assimilate atmospheric N2?
Glutamine Synthetase/GOGAT
glu + NH3 --(GS)--> gln
gln + a-ketoglutarate --(GOGAT)--> 2 glu

Glutamate Dehydrogenase
a-ketoglutarate --> glu
How do bacteroids feed nitrogen to the host plant?
What exchange occurs between bacteroids and host plants?
Plant gives: TCA Cycle intermediates, sugars, organic acids

Bacteroid gives: gln, asn
What do bacteroids do with TCA cycle intermediates from the plant?
Run TCA Cycle --> Generate reducing power for ETChain --> ATP
What triggers the A Signal in myxobacteria and what does it do?
C/N/P Starvation --> ppGpp made --> A signal released (small peptides)

A signal functions as a quorum sensor. Once critical concentration is reached SasR initiates transcription of FruA.
What is the function of C Signaling?
Coordinates cell movement and aggregation, triggers phosphorylation of FruA

FruA-P --> aggregation, streaming, myxospore formation
Describe the mechanism involved in myxobacterial social motility.
Used by rafts of 15-20 cells traveling in a wave.

Type IV Pili: 2 ATP Driven motors
PilB - extends pilus by adding pilin units to base
PilT - retracts pilus by removing pilin units from base.

Works like grappling hook: reel self forward
Describe the mechanism involved in myxobacterial adventurous motility.
Secretion of "slime jets"

or cytoskeletal proteins may adhere to the surface and be used to corkscrew the cell forward across the medium.
What is the function of Nod factors?
Secreted by Rhizobial cells to encourage curling of root hair + increased plant cell division --> nodule formation
What class of compounds do root hairs secrete to attract Rhizobial cells?

Can attract/deter: produce selectively to direct infection to specific areas of plant.
What helps to ensure host plant/Rhizobial species specificity?
Ca-Binding Proteins: binds Ca on root tip
Lectins: adhere to specific polysaccharides on root hair.
Flavonoids: plant flavonoids will only attract certain Rhizobial cells.
What is homologous recombination?
Exchange of homologous regions of ssDNA on 2 DNA molecules --> heteroduplex

Next round of replication --> 2 different genomes:
1. original genome
2. strand of DNA that has the exchanged part in it
What is nonhomologous recombination?
Exchange of nonhomologous or unevenly sized regions of ssDNA --> 1 genome with gene deletions, 1 genome with gene duplications.

May also put incorrect gene under control of wrong promoter.
What base does 5-Bromouracil substitte for?
Subs for Thymine but pairs with Guanine, not Adenine

A/T --> 5-Br Uracil/G --> C/G Base pair
What is the most damaging effect of ionizing radiation?
Breaks P-O-P DNA backbone --> may linearize chromosome.

Creates AP sites by detaching bases
What is the difference between Insertion Sequences and Transposons?
Length and Genetic content

IS = smaller, 800-2000bp, only transposase gene

Tn = larger >2000bp, caries transposase + other genes (ex. antibiotic resistance), flanked by IS on either side.

Both flanked by palindromic sequences.
What are the two modes of transposition?
Replicative: Tn/IS replicates self and inserts copy in new location.

Nonreplicative: "cut and paste" IS/Tn excises and reinserts self elsewhere.
Why are IS/Tn's problematic?
They can insert themselves in the middle of a gene --> interrupt gene --> nonfunctional protein
What is a nonsense mutation?
Change that results in a STOP codon --> early termination of peptide synthesis

Severity of effect depends on where peptide got truncated
What is a missense mutation?
Switch in 1st or 2nd letter of codon --> different/wrong AA inserted
What is a frame shift mutation?
Deletion/Insertion of bases in a number that is NOT a multiple of 3

--> reading frame shift. every codon downstream of mutation is ruined

necessarily fatal for the peptide.
What is light repair and what does it fix?
Repairs thymine dimers due to UV light

Photolyase enzyme: uses light E to break thymine dimers apart.
What is Damaged Base Repair and what does it fix?
repairs modified bases.

-Enzyme detaches base from ribose --> AP site
-AP endonucleases excise portion of DNA surrounding AP site
-DNA Pol I + Ligase repair.
What is Dark/Nucleotide Excision repair and what does it fix?
Fix: damaged regions of DNA

UrvABC protein complex
-Nicks DNA 8bp 5' of damage, 4-5bp 3' of damage
-Helicase unwinds + removes damaged region
-DNA Pol I + Ligase repair.
What is Recombinational/Post-replication Repair and what does it fix?
Fixes when DNA Pol III had to skip replicating a damaged region of DNA --> region of damaged ssDNA remains on chromosome

-RecA protein excises homologous ssDNA from new sister chromosome
-RecA and Ligase insert borrowed strand into damaged unreplicated chromosome for DNA Pol to use as template.
How does the Methyl Directed Mismatch Repair system work?
Dictates which base is wrong in a mismatched bp.

-MutS: looks for + binds damaged DNA
-MutH: binds nearest -CH3 grp to MutS
-MutL: binds MutS + MutH, uses ATP to nick nonmethylated strand
-ssDNA exonuclease cuts out damaged region
-DNA Pol I/Ligase repair.
What is SOS repair and what does it fix?
SOS repair = last ditch effort when all other repair mechanisms are saturated.

-LexA protein represses repair enzyme operons and error prone DNA Pol operons.
-RecA protein: Inactivates LexA repressor --> increased repair enzyme expression BUT also increased error prone DNA Pol IV + V.
What is the average spontaneous mutation rate in bacterial genes?
~1 mutation per 1,000,000 cell divisions

What is one advantage of a high mutation rate (as in mutator strains)?
Allows bacteria a better chance to adapt to a quickly changing environment. Higher SMR --> more mutations --> more chances for a favorable adaptation.
In MCP-directed chemotaxis, what happens upon addition of an attractant?
Attractant binds Chemosensor (binding protein)

Sensor/Attractant binds MCP

MCP --> conf. change that allows methylation

CheR methylates slowly.
Why is the adaptation period slow and transient?
CheR methylates MCP II slowly.

Transient because once appropriate level of methylation is reached or levels of attractant become stable, CheR stops methylating.

Cell resumes unbiased random run/tumble frequency until environment changes.
Why is the chemotactic de-adaptation period so much shorter than the adaptation period?
CheB, which de-methylates MCP II, acts much more quickly than CheR did.
How do cells involved in chemotaxis compare their past and present environments?
Compare the level of association of MCP II with attractant/binding protein to level of MCP II methylation.

Assoc. w/binding protein is instantaneous and reflects present environment; methylation is slow and reflects past.
When does CheA autophosphorylate itself?
In the presence of unfavorable environmental conditions: no attractant or presence of repellent.

CheA-P transfers P to CheY so it can trigger CW flagellar rotation --> cell tumbles.
How does the Phosphotransferase System regulate chemotaxis?
Levels of phosphorylation of Enzyme I measure concentration of PTS substrate.

High substrate --> low Enzyme I-P levels inhibit CheA.

Less CheA-P --> Less CheY-P --> Less CW rotation/tumbles; cell has longer runs.
Which Che proteins are involved in termination of chemotactic response?
CheA-P --> phosphorylate CheB and CheY
CheB-P --> de-methylate MCP II
CheY-P --> CW flagellar rotation (tumble)
Why is liver extract added to chemicals being subjected to the Ames test?
Liver makes mixed function oxygenases which often convert chemicals in to mutagens or carcinogens.
What is the basis of the Ames test for mutagen/carcinogenicity?
Growth of a supposedly auxotrophic mutant indicates mutation back into prototrophs.

More mutations = more prototrophs = more growth.

So level of growth is proportional to mutagenicity of compound in question.